HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations
| Autor: | Sandrine Lecour, Gaurang Deshpande, M. Faadiel Essop, Leanne Dominick, Natasha Driescher, Etheresia Pretorius, Theo Nell, Eman Teer, Richard H. Glashoff, Nicholas J. Woudberg, Natasha Midgley, Martin J. Page, Danzil E. Joseph |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Physiology Human immunodeficiency virus (HIV) HIV Infections 030204 cardiovascular system & hematology Lymphocyte Activation medicine.disease_cause Monocytes Subclass 0302 clinical medicine Risk Factors T-Lymphocyte Subsets biology Diseases onset Forkhead Transcription Factors Middle Aged Lipids medicine.anatomical_structure Coagulation Cardiovascular Diseases Female Cardiology and Cardiovascular Medicine Lipopolysaccharide binding protein Adult Anti-HIV Agents T cell Antigens Differentiation Myelomonocytic Receptors Cell Surface Thromboplastin 03 medical and health sciences Antigens CD Physiology (medical) medicine Antiretroviral treatment Humans Blood Coagulation Cell Proliferation Monocyte subsets business.industry Membrane Proteins Matrix Attachment Region Binding Proteins Macrophage Activation Cross-Sectional Studies 030104 developmental biology Case-Control Studies Immunology biology.protein business Biomarkers |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 316:H1146-H1157 |
| ISSN: | 1522-1539 0363-6135 |
| Popis: | Although rollout of combined antiretroviral treatment (cART) has blunted human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) onset, there is increased development of cardiovascular diseases (CVDs) in HIV-infected individuals. While most HIV-infected individuals on cART achieve viral suppression, this may not necessarily result in complete immunological recovery. This study therefore evaluated T-cell-mediated changes and coagulation markers in HIV-positive individuals to ascertain their potential to increase CVD risk. Eighty participants were recruited (Worcester, South Africa), and fasted blood was collected to evaluate: 1) immune activation (CD38 expression on CD4+and CD8+T cells) and thrombus formation [tissue factor (CD142)] on CD4+and CD8+T cells; 2) monocyte subpopulations (nonclassical, intermediate, and classical); and 3) classical regulatory T (Treg) cells with activation markers [glycoprotein A repetitions predominant (GARP) and special AT-rich sequence-binding protein 1 (SATB-1)]. High- and low-density lipoprotein subclasses (Lipoprint) were also determined. This study revealed four key findings for HIV-positive patients: 1) coexpression of the CD142 coagulation marker together with immune activation on both CD4+and CD8+T cells during chronic infection stages; 2) Treg cell activation and upregulated GARP and SATB-1 contributing to Treg dysfunction in chronic HIV; 3) proatherogenic monocyte subset expansion with significant correlation between T-cell activation and macrophage activation (marker: CD163); and 4) significant correlation between immune activation and lipid subclasses, revealing crucial changes that can be missed by traditional lipid marker assessments (LDL and HDL). These data also implicate lipopolysaccharide-binding protein as a crucial link between immune activation, lipid alterations, and increased CVD risk.NEW & NOTEWORTHY With combined antiretroviral treatment rollout, HIV-AIDS patients are increasingly associated with cardiovascular diseases onset. This study demonstrated the significant interplay between adaptive immune cell activation and monocyte/macrophage markers in especially HIV-positive individuals with virological failure and on second line treatment. Our data also show a unique link between immune activation and lipid subclass alterations, revealing important changes that can be missed by traditional lipid marker assessments (e.g., LDL and HDL). |
| Databáze: | OpenAIRE |
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